0000000000359846

AUTHOR

Elena D'amato

showing 2 related works from this author

Enhanced glomerular Toll-like receptor 4 expression and signaling in patients with type 2 diabetic nephropathy and microalbuminuria

2014

Toll-like receptor 4 (TLR4), a component of the innate immune system, is recognized to promote tubulointerstitial inflammation in overt diabetic nephropathy (DN). However, there is no information on immune activation in resident renal cells at an early stage of human DN. In order to investigate this, we studied TLR4 gene and protein expression and TLR4 downward signaling in kidney biopsies of 12 patients with type 2 diabetes and microalbuminuria, and compared them with 11 patients with overt DN, 10 with minimal change disease (MCD), and control kidneys from 13 patients undergoing surgery for a small renal mass. Both in microalbuminuria and in overt DN, TLR4 mRNA and protein were overexpress…

MaleKidney GlomerulusDiabetic nephropathyurologic and male genital diseasesDiabetic nephropathynefropatiadiabeticaDiabetic NephropathiesMinimal change diseaseChemokine CCL5KidneyMiddle AgedUp-RegulationKidney Tubulesmedicine.anatomical_structureNephrologyDisease ProgressionFemaleHumanSignal Transductionmedicine.medical_specialtyReceptors CCR5Receptors CCR2NephrosisAntigens Differentiation MyelomonocyticFollow-Up StudieNephropathyToll-like receptorAntigens CDDiabetes mellitusInternal medicinemedicineAlbuminuriaHumansRNA MessengerInflammationInterleukin-6Tumor Necrosis Factor-alphabusiness.industryNephrosis LipoidKidney TubuleTranscription Factor RelABiomarkermedicine.diseaseImmunity InnateToll-Like Receptor 4EndocrinologyDiabetes Mellitus Type 2Diabetic NephropathieTLR4MicroalbuminuriaKidney GlomerulubusinessBiomarkersMicroalbuminuriaFollow-Up StudiesKidney International
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Lysine triggers apoptosis through a NADPH oxidase-dependent mechanism in human renal tubular cells

2012

Progressive chronic kidney disease (CKD) is common in lysinuric protein intolerance (LPI), a primary inherited aminoaciduria characterized by massive Lysine excretion in urine. However, by which mechanisms Lysine may cause kidney damage to tubule cells is still not understood. This study determined whether Lysine overloading of human proximal tubular cells (HK-2) in culture enhances apoptotic cell loss and its associated mechanisms. Overloading HK-2 with Lysine levels reproducing those observed in urine of patients affected by LPI (10 mM) increased apoptosis (+30%; p < 0.01 vs.C), as well as Bax and Apaf-1 expressions (+30-50% p < 0.05), while downregulated Bcl-2 (-40% p < 0.05). Apoptosis …

medicine.medical_specialtyLysineGene ExpressionApoptosisNADPH Oxidasecomplex mixturesAntioxidantsCell LineExcretionKidney Tubules ProximalInternal medicineGeneticsmedicineHumansRenal Insufficiency ChronicAmino Acid Metabolism Inborn ErrorsProtein SubunitGenetics (clinical)Membrane Potential MitochondrialKidneyNADPH oxidasebiologyLysineAmino Acid Metabolism Inborn ErrorNADPH OxidasesApoptosimedicine.diseaseCaspase InhibitorsLysinuric protein intoleranceIn vitroProtein SubunitsEndocrinologymedicine.anatomical_structureCell cultureApoptosisbiology.proteinCaspase InhibitorDisease ProgressionAntioxidantReactive Oxygen SpeciesReactive Oxygen SpecieHuman
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